Neurology Flashcards
What are the causes of Virtigo?
Benign paroxysmal positional vertigo. Acute labyrinthitis Meniere's Disease Ototoxicity Acoustic Neuroma Herpes Zoster Traumatic damage Stroke/TIA Migraine Alcohol intoxication
What is BPPV? It’s cause and symptoms?
Condition that causes sudden onset of dizziness associated with head movement.
Causes - usually idiopathic. If young = trauma.
Symptoms - Episodic (10-20 secs) virtigo associated with change of head position. Can be associated with nausea
What features are not associated with BPPV?
Tinnitus
Hearing Loss
Investigations for BPPV?
Family history of RA / back pain - may complicated further examinations
Ear examination
Dix-Hallpike test -
Management of BPPV?
Watch and wait - is this acceptable for the patient?
Epley manoeuvre
Consider Brandt-Daroff exercises. (vestibular rehabilitation)
Betahistine is commonly used (histamine analogue) but not very effective.
What is a Dix-Hallpike test and what is it used for?
Test for BPPV.
Patient sites up, turns head 45o in one direction. Lower patient in this position, make sure head is 30o below horizontal. Observe for rotatory nystagmus and vertigo.
Should be performed, tilting the head both left and right.
What is the Epley Manoeuvre and what is it used for?
Used for the management of BPPV.
With patient lying down, rotate head 90o. Ask patient to turn to that side whilst lying down. Turn head 90o so the head is facing the floor. Ask patient to sit up maintaining the direction of the head tilt. Realign head and flex neck downwards.
What is meniere’s disease and what are the symptoms?
Disorder of the inner ear. Characterised by pressure and dilatation of the endolymphatic system.
Symptoms - recurrent episodes of vertigo (>20 mins each), tinnitus and hearing loss (sensorineural). Vertigo is usually the prominent symptom
a sensation of aural fullness or pressure is now recognised as being common
nystagmus and a positive Romberg test
episodes last minutes to hours
typically symptoms are unilateral but bilateral symptoms may develop after a number of years
What is the classic triad of meniere’s disease?
Vertigo (recurrent)
Tinnitus
Fluctuating hear loss
Usually unilateral
Investigations for meniere’s disease?
ENT assessment to confirm diagnosis.
Refer to audiology
Admit if symptoms severe - IV labyrinthine sedatives (meclozine, promethazine) and fluids.
Second line - Diazepam or Prochlorperazine.
Betahistine for prevention.
Reassurance. Inform the DVLA.
What is acute labyrinthitis and what are its symptoms?
Also known as vestibular neuonitis.
Vertigo following a viral infection.
Features - Abrupt onset of severe vertigo (recurrent, lasting hours), nausea and vomiting.
Horizonal nystagmus is common.
NO DEAFNESS OR TINNITUS.
What is the treatment of acute labyrinthitis?
Vestibular rehabilitation exercises for those with chronic symptoms.
Buccal or IM prochlorperazine for those with acute severe symptoms.
Less severe = proclorperazine or anti-histamines.
What is acoustic neuroma and what are the symptoms?
Schwannoma from the vestibular nerve (rare tumour of the nervous system).
Growth rate = 1mm/year
Tumours slow growing and often benign
Symptoms - unilateral hearing loss with vertigo occurring later. Progressive = cranial nerves affected -V (absent corneal reflex), VI, IX, X) Raised ICP if advanced. Bilateral = NF2
Acoustic Neuroma treatment.
Refer urgently to ENT.
Surgery, radiotherapy or observation.
Acoustic Neuroma Investigation
ENT referral (Urgent) MRI of cerebellopontine angle is investigation of choice Audiometry is important. (
Syncope differentials
Reflex (vasovagal, situational, carotid sinus hypersensitivity, atypical) Orthostatic hypotension Cardiac syncope (arrhythmia, structural heart disease)
Common examinations for syncope.
Cardiac examination
ECG (including 24h)
Blood pressures (standing up and lying down)
Table tilt test
What is vasovagal syncope, signs, management?
Type of reflex syncope. Most common cause of fainting.
Caused by emotional distress (prolonged standing in heat). Common in young adults/adolescents.
Classic faint.
Benign - reassurance and trigger recognition. Avoid BP lowering agents.
Cardiac syncope. Causes, investigations, management.
Causes - arrhythmias, bradycardia. Can also be tachycardia.
Structural - Hypertrophy, valvular, MI
Others - pulmonary embolism.
Cardio examination ECG 24 hr ECG U&E's, FBC, Ca2+, glucose Echo CT/MRI brain ABG (pulmonary embolism, low CO2 suggests hyperventilation)
How do you classify epilepsy?
Either by seizure types of epilepsy syndrome.
Seizure types - Focal (starts in one place but can spread), generalised (both hemispheres affected).
Epilepsy syndrome - juvenille, Dravets
Focal seizure classifications.
Without impairment of consciousness or with.
Frontal movements - posturing (prolonged extension or flexion of the limbs) or peddling. Motor arrest subtle behavioural changes. Language can be affected as well.
Parietal - sensory disturbances such as tingling, numbness or pain
Can also have motor symptoms (if spread to the pre-central gyrus)
Temporal - automatisms (complex motor phenomena with unconsciousness - lip-smacking, chewing, swallowing)
Deja Vu
Emotional disturbance - tremor, panic anger
Hallucinations - smell, taste sound
Occipital - Visual disturbances (spots, lines, flashes)
General seizure classifications
Tonic-clonic - loss of consciousness, limbs stiffen (tonic), then jerk (clonic)
Absence seizure - begin in childhood, sharp onset and offset, eyelid twitching.
Myoclonic - shock-like contraction of the limbs, without impairment.
Atonic - sudden loss of muscle tone causing falls.
Diagnosis of Epilepsy
All patients with a seizure must be referred to specialist.
Take a thorough examination and establish the type of seizure.
Rule out provoking causes - trauma, stroke, haemorrhage, raised ICP, alcohol or benzodiazepine withdrawal
Metabolic causes - hypoxia, hypernatraemia, hypocalcaemia, hyperglycaemia.
Infection - meningitis
Drugs - cocaine, tryclyclics.
Investigations - Bloods (see for above). ECG. Consider EEG
MRI - structual cause
Drug levels - anti-eplieptic medication
DVLA
Headache differentials
Tension headache Glaucoma Migraine Trigeminal neuralgia Cluster headache Meningitis Sinusitis Head injury (extradural, subdural, subarachnoid)
Characteristics and management of a tension headache
“tight band across the forehead. Symptoms tend to be bilateral.
Lower intensity than a migraine. Also no aura, N+V
May be related to stress.
Other triggers: Dehydration, alcohol, skipping meals
Can coexist with a migraine.
NICE - Acute = aspirin, paracetamol or NSAID as first-line.
Prophylaxis - 10 sessions of acupuncture over 5-8 weeks
Low-dose amitryptyline
Above is for chronic tension-type (occuring 15 days or more per month)
Characteristic of a cluster headache (+risk factors)
Intense pain around the eye.
Usual presentation is a headache and a red, watery eye with nasal congestion/rhinorrhoea
Other symptoms - Lacrimation, eyelid oedema, facial/forehead sweating, miosis (constriction) and/or ptosis
Frequency - 1 every other day - 8 times a day
Clustered for 6-12 weeks followed by pain free periods
Most commonly affects men in their 20s or older who are smokers, family history, male sex and smoking/alcohol are risk factors.
Management of a cluster headache
C - reassurance, lifestyle changes - alcohol and smoking avoidance (triggers)
M - Acute Attacks - 100% oxygen (15 min via non-rebreather) - caution if COPD and subcut sumatriptan
Prophylaxis - Verapamil or prednisolone
S - Not much place but optical nerve stimulation may have a role in preventative medically-refractory chronic cluster headaches. (very last line management)
Differentials / investigations of a cluster headache
Migraine Paroxysmal hemicrania Trigeminal neuralgia Giant cell arteritis Headache associated with sexual activity Angle-closure glaucoma
Brain CT / MRI - rule out secondary causes (tumour, cavernous sinus pathology) (normal in cluster)
ESR - Exclude giant cell arteritis if over 50.
Pituitary function tests ?
Trigeminal Neuralgia Symptoms, investigations
Facial pain syndrome in the distribution of 1 or more divisions of the trigeminal nerve.
Symptoms - paroxysms of intense, stabbing pain lasting seconds in the trigeminal nerve area (V2 and V3). Face screws with pain.
Triggers - washing affected area, shaving, eating, talking
Typically male >50.
AGE AND MS are risk factors.
Investigations - clinical diagnosis THINK SECONDARY CAUSES = intra-oral X-ray (if dental cause suspected - dental caries, fracture). MRI - tumour, infarct, MS plaque
Trigeminal Neuralgia management
Medical preferred:
Anticonvulsants - Carbamazepine 1st line
2nd line - Topiramate
3rd line - gabapentin, lamotrigine
Consider baclofen (anti-spasmodic if resistant to the above)
For medically resistant - surgery = microvascular decompression (surgery to the compressive loop)
Migraine Presentation
Chronic, genetically determined, episodic neurological disorder that usually presents early-to-mid life.
Risk factors - family history, childhood motion sickness, caffeine, high altitude, female sex, menstruation, divorced, widowed or separated. Stress, overuse of headache medication, lack of sleep.
Prolonged headache - unilateral often. Throbbing/pulsing. Aura (blurred visiob) Hemiplegic disabling Lasts 4-72 hours Photophobia N+V Associated with triggers - worse with activity, caffeine, sex, chocolate, dehydration
Investigations for a migraine
Clinical diagnosis
ESR - rule out temporal arteritis (>50)
LP - abnormal if caused by subarach, meningitis,
MRI Brain (with contrast) - recommended for all concerning headaches. - may identify space occupying lesion or ischaemia
CT without contrast - emergency evaluation of acute headache (evaluate for intracranial haemorrhage)
Acute Migraine Management
Mild-moderate = NSAIDs / paracetamol + anti-emetic (metoclopramide), hydration
Severe = Triptan (almotriptan, sumatriptan). + same as above
IF PREGNANT = PARACETAMOL, ANTI-EMETIC, HYDRATION, MAGNESIUM
A+E severe = rescue therapy - metoclopramide or prochlorperazine + dipenhydramine or triptan + oxygen + IV corticosteroid
Ongoing Migraine Management
C - trigger avoidance and behavioural modification (relaxation/CBT), avoid caffeiene, cheese, chocolate etc.
M - NON-PREGNANT - cycle control (hormonal therapy if menstrual associated). Magnesium, triptan (frovatriptan or zolmitriptan) ?? or is it topiramate
Basically - propranolol, amitriptyline, or topiramate
verapamil (for hemiplegic migraine)
Red Flags for Headaches
New onset in > 50 years old Immunocomprimised History of malignancy known to metastasis to the brain Vomiting Impairment of consciousness Thunderclap Focal neurological symptoms Change in characteristic Abnormal neurological examination Headache with changes in posture Jaw claudication Neck stiffness Fever Personality change
Head Injury Approach
PROTECT AIRWAY AND C-SPINE Oxygen if sats <92% Stop blood loss Treat seizures with phenytoin Assess consciousness - intubate if GCS < 8 Neuro examination History Check for CSF leak from nose/ear
What are the indications for CT Head Immediately following a Head Injury (<1 HR)?
GCS < 13 on assessment GCS < 15 after 2 hours Suspected open or depressed skull fracture Sign of basal skull fracture Post-traumatic seizure Focal neurological deficit >1 episode of vomiting
What are the indications for CT Head within 8 hours following a Head Injury?
Age > 65
History of bleeding or clotting disorder
Dangerous mechanism of injury (pedestrian / cyclist hit by a car)
>30 mins of retrograde amnesia immediately before head injury.
Patient on warfarin.
Presentation of Extradural haemorrhage.
Typically trauma. Lucid interval.
Typically - initial loss of consciousness, briefly regains and then loses again.
Fixed, dilated pupil due to uncal herniation causing compression on third cranial nerve
Signs of raised ICP. Headache. Confusion, seizures, UMN signs. Dilated pupil (ispilateral)
What is an extradural haemorrhage and how are they sustained?
Collection of blood between the skull and dura.
Almost always caused by trauma (low-impact trauma).
Usually in the temporal area (pterion overlies the middle meningeal artery which is therefore vulnerable).
Investigations for Extradural haemorrhage
ABCDE Bedside obs Assess GCS Bloods - coag CT HEAD Biconvex/lens shaped, hyperdense collection around the surface of the brain, limited by suture lines of the skull
Management of extradural haemorrhage
ABCDE
Stablise - protect airway and C-spine
Transfer to neurosurgery for clot evacuation / ligation of bleeding airway
Mannitol to reduce ICP
What is a subdural haematoma, risk factors and how are they caused?
Collection of blood beneath the dural layer of the meninges.
Risk factors: 3A’s - Age, Alcohol and Anticoagulation (also coagulopathy)
Cause: High impact trauma, can therefore be associated with underlying brain injury.
Presentation of a subdural haematoma
Ranges from incidental finding to coma and coning (due to herniation)
Headache - gradually gets worse over hours-days
N+V
Diminished GCS
Losing consciousness
Seizures, sensory changes if getting worse
Signs of raised ICP
Investigations for a subdural haematoma
ABCDE
Basic obs / GCS
Non-contrast CT (standard choice in suspected haematoma). - will see a crescent shape collection of blood (not limited by suture lines). May also be midline shift
Consider MRI - assess extent of brain injury
Management of a subdural haematoma
ABCDE
Incubate if GCS < 8
Analgesia (pain can increase ICP)
Neurosurgical referral if persistent symptoms after initial assessment, focal neurological deficit or significant findings on CT.
If small haematoma (<10mm) and midline shift <10mm then observation, monitoring and follow up.
Prophylactic anti-emetics
Correction of coagulopathy
If large (>10 mm) or midline shift >5 mm then surgery - burr hole cranitomy.
Chronic - antiepileptics, elective surgery and coagulopathy correction.
Consider conservative - fall management, avoid activities that risk injury, controlled return to normal activities, having someone at home within first 24 hours to observe them.
What is stroke, the main types and the causes?
Stroke - rapid neurological deficit resulting from altered blood supply to the brain lasting > 24 hours
Types - Ischaemic, haemorrhagic (+TIA)
Ischaemic - 85% of strokes, emboli, typically arising from the heart (AF/MI/Valve disease), aortic arch, carotid artery (atheroma)
Haemorrhagic - intraparenchymal, subarachnoid. Cause - Vascular abnormality (aneurism), coagulopathy, vasculitis
Signs / symptoms of stroke
FAST Focal neurological signs - weak, numb Hemiplegia Sudden onset - often from waking up Symptoms worsen within hours Problems with speech Balance problems Also signs of source of emboli (ischaemic stroke) - murmur, fever (infective endocarditis, valve disease)
3 things to lookout for to help classify strokes?
Unilateral hemiparesis and/or hemisensory loss of face, arm or leg (UMN signs)
Visual signs - particularly homonymous hemianopia
Higher cognitive dysfunction - dysphagia, aphasia
Total Anterior Circulation Stroke (TACS) cause and presentation
Cause - occlusion of the internal carotid, cerebral or anterior cerebral arteries
Presentation - unilateral hemiparesis
Homonymous hemianopia
Higher cognitive dysfunction (dysphasia, aphasia)
Stroke investigations
Bloods - FBC, platelets, ESR, U+Es and LFTs, coag, glucose, cholesterol (know why we do these - notes)
CV tests - ECG, CXR, Echo, carotid duplex US
EMERGENCY NEUROIMAGING - CT (rules out haemorrhage and tumour but may be initially normal on an ischaemic stroke, also allows thrombolysis)
CT angiography (large vessel occlusion)
MRI - more sensitive than CT but less available
Stroke Management
ABCDE
Prevent hypoxia, hypoglycaemia, hypotension and infection
DVT prophylaxis if immobile
Admit to specialist stroke ward
MDT - physio, OT, speech and language therapy
Ischaemic - Thrombolysis if 4.5 hours of onset of symptoms and patient has not had previous haemorrhage or pregnant or uncontrolled HTN
Thrombectomy - if large vessel occlusion
Antiplatelets - Aspirin 300 mg OD for 24 hours post thrombolysis. Continue for 2 weeks before switching to long-term antiplatelet.
Haemorrhagic stroke - neurosurgical referral
Secondary Prevention - Antiplatelet (clopidogrel 1st line followed by Aspirin + modified-release dipyridamole 2nd line).
Anticoag instead for anti-platelet if AF
Statins for all
Screen and treat HTN
Carotid endarterectomy or stentin if > 50% carotid stenosis
Lifestyle changes
When can you give thrombolysis for a stroke?
Haemorrhagic stroke excluded.
Patient presents within 4.5 hours on symptom onset
No previous intracranial haemorrhage, uncontrolled HTN or pregnant
Also no CI to thrombolysis
Thrombolysis = Alteplase or Tenecteplase
Multiple Sclerosis Presentation
Optic Neuritis - ranges from reduced vision and colour blindness to complete vision loss. May see RAPD, disc swelling
Transverse myelitis
Other: - Dysaesthesia (feeling like water trickling or electric shock). Motor - spastic weakness, cerebellar symptoms, dysphagia, constipation, fatigue, cognitive impairment
As MS becomes progressive - gradual accumulation of disability
Multiple Sclerosis Investigations
MRI brain and spinal cord - Plaques: Hyperintense lesions on T2-weighted MRI or enhancement of active lesions with gadolinium-enhanced T1 MRI.
CSF - Oligoclonal IgG bands on electrophoresis which are not found in serum
Also increased protein and WBC (but less common)
McDonald Criteria
Other:
FBC, CRP - signs of inflammatory disease
B12 - cause for neurological symptoms
TSH - eye disease
U+Es - for electrolyte neurological symptoms
Glucose - for diabetes causing neuropathy and eye disease
HIV - various neurological manifestations
What is the McDonald Criteria?
Used in MS for diagnosis
> 2 or equal to 2 attacks, disseminated in time (>30 days) and place (>2 areas of CNS), not explained by anything else
Diagnosis can be purely clinical, provided there are objective neurological findings for at least 1 attack and attacks last >24 hours
Radiological diagnosis requires 2 lesions
Describe the management of status epilepticus
ABCDE
IV access - bloods = FBC, toxicology screen, LFTs, glucose, U+E, calcium
Give IV glucose, thiamine or fluids as required
Give IV lorazepam (or rectal if pre-hospital) - ideally in slow bolus (30s)
Repeat after 10 mins if required
Ongoing seizure (20 mins) - phenytoin loading dose
Seizure ongoing (30 mins) - general anaesthesia with prenobarbital or propofol.
Presentation of Meningitis
Classic triad - fever, headache, neck stiffness Photophobia LOC Drowsiness N+V Could be associated with a recent URTI Rash (invasive meningococcal infection) Seizures
Meningitis CSF Profile:
Yellow Polymorphonuclear cells - slightly increased Lymphocytes - markedly increased Protein - increased Glucose - decreased
Infection?
Tuberculosis (bacterial = polymorphonuclear cells would be markedly increased
Viral = clear fluid, normal glucose (or slightly decreased). Normal protein
What is syringomyelia and how does it present?
Development of fluid-filled cyst (syrinx) within the spinal cord. Typically develop due to blocked CSF flow (commonly associated with a Chiari malformation)
Presentation - mean age of diagnosis = 30 years
Dissociated sensory loss - absent pain and temperature sensation with preserved light touch, vibration and joint position sense. Distribution depends on position of the Syrinx (affecting a certain root distribution)
Typical cervical syrinx - sensory loss over trunk and arms
Also - wasting of the hands, claw hand
Can also have Horner’s syndrome (bilateral) UMN leg signs.
First line drug for focal seizures
Carbamazepine
Management of status epilepticus
ABCDE
IV access- bloods - glucose, calcium u/es, LFT, FBC,
First line drugs are benzodiazepines
- diazepam (pre hospital rectally)
- lorazepam 4mg repeated after 10 minutes if the seizure continues
20 mins - phenytoin
30 mins - general anaesthesia (propofol)
Presentation of hydrocephalus
Raised ICP Headache N+v Visual problems Normal pressure - urinary incontinence, dementia and gait disturbance
Classification of hydrocephalus
Communicating - impaired absorption of CSF, no obstruction (SAH, meningitis)
Non-communicating - OBSTRUCTIVE - congenital abnormalities (arnold-Chiari) - bleeding, tumour
Normal pressure - dilated cerebral ventricles
Presentation of intracranial venous thrombosis
Most commonly occur in sagittal sinus thrombosis
- headache, vomiting, seizures, decreased vision, papilloedema
Causes of venous sinus thrombosis
Numerous - anything that puts someone in a hypercoagulable state
Common- pregnancy, COCP, head injury
Dehydration
Investigations of dural sinus thrombosis
Exclude SAH and meningitis
Thrombophilia screen
Imaging - CT/MRI venography
LP - raised opening pressure, may show RBCs or be normal
Management of dural sinus thrombosis
Anticoagulation with heparin or LMWH
Still deterioration - endovascular thrombolysis or mechanical theombectomy
Raised ICP - decompressive hemicraniectomy
Features of motor neuron disease
Think of in >40 years old with stumbling spastic gait, foot drop, proximal myopathy
Mixed UMN and LMN signs
Speech and swallowing affected? Bulbar palsy
Does not cause sensory loss or sphincter disturbance
Wasting of small muscles of hands is common
Also frontotemporal dementia occurs
Degenerative cervical myopathy presentation
Caused by pressure in the neck
Early symptoms are subtle then progress
Pain in neck, upper and low limbs
Loss of motor function - digit dexterity, doing up shirt etc.
Loss of sensory function - numbness
Loss of autonomic function- urinary/faecal incontinence
Hoffmans sign - flicking one finger causes reflex twitching in the opposite
Management of degenerative cervical myelopathy
Specialist spinal services
Early treatment needed
Decompressive surgery
Classic triad of parkinsons
Resting tremor
Rigidity
Bradykinesia
Classic triad of parkinsons
Resting tremor
Rigidity
Bradykinesia
Do tremors improve or get worse with movement?
Improves
Tremors more pronounced while resting or distracted (ask them to do a task with other arm)
Features of parkinsons
Bradykinesia Tremor at rest Shuffling gait Rigidity Flexed posture Depression Sleep disturbance Loss of snell
Carbidopa and benserazide are examples of what drugs
Decarboxylase inhibitors
- given in parkinsons to prevent dopamine being broken down. Given with levodopa
First line management in parkinsons
Levodopa and dopa decarboxylase inhibitors
Symptoms of multiple system atrophy
Parkinsons
Autonomic dysfunction
- postural hypotension
- constipation
- urinary symptoms
- sweating
- sexual dysfunction
- ataxia
What time frame should thromectomy be offered
Within 6 hours
Not used after 24 hours
Secondary prevention of stroke
Antiplatelet - 75mg clopidogrel
If not acceptable or CI
- aspirin plus modified-release dipyridamole
Presentation of gullian-barre syndrome
Features of infection 2-4 weeks prior
- symmetrical ascending weakness
- reduced reflexes
- peripheral loss of sensation and neuropathic pain
- cranial involvement - diplopia, bilateral facial nerve palsy
- autonomic - urinary retention
- LMN signs
Diagnosis of gullian-barre syndrome
Usually made clinically
Brighton criteria
Nerve conduction studies - reduced signal
Lumbar puncture for CSF - raised protein with a normal cell count
Management of gullian-barre syndrome
IV immunoglobulin Plasma exchange Supportive care VTE prophylaxis - PE biggest killer Respiratory failure - intubation and ventilation
When should prophylaxis for migraine be given, drugs used?
2 or more attacks per month
Topiramate or propranolol
Not topiramate in child bearing age in women
If these fail - acupuncture Also riboflavin (B2)
Predictable menstrual migraine - frovatriptan or zolmatriptan
First line radiographic investigation in stroke
CT head
- rules out haemorrhagic
Contents of the cavernous sinus
Lateral wall components
- oculomotor nerve
- trochlear nerve
- opthalmic nerve
- maxillary nerve
Contents of the sinus
- internal carotid artery
- Abducens nerve
Presentation of cavernous sinus syndrome
Opthalmoplegia (CN III, IV, VI) Autonomic dysfunction (horners) Sensory loss (trigeminal neuralgia)
Different from posterior communicating artery aneurysm - ptosis and dilated pupil
Cavernous sinus - absent corneal reflex and proptosis
Managemeng of epilepsy
Most forms - sodium valproate
Focal - carbamazepine
Generalised 2nd line - lamotrigine
Absence - sodium valproate, ethosuximide
Myoclonic - 2nd line - clozipine, lamotrigine
Focal - 2nd line - levetiracetam
Risk factors for IIH
Female sex
Obesity
Sleep apnoea
Drugs - COCP, steroids, vitamin A, lithium
Presentation of IIH
Headache Blurred vision Papilloedema Photophobia 6th nerve palsy Visual field loss
Management of IIH
First line
- weight reduction
- eliminate causes - TCAs, retinoids, vitamin A
- low sodium diet
Medical
- diuretics- acetazolamide, furesomide
- topiramate
- repeated lumbar puncture
Surgical
- CSF shunting
What is neurofibromatosis
Condition where tumours grow on nervous tissue
They can develop anywhere in the NS (brain, spinal cord and nerves)
Neurofibromatosis 1 vs 2
1
- cafe su last spots at least 6
Axillary and groin freckles
Iris haematomas
2
- bilateral vestibular schwannomas
- fewer cafe au last spots
- tinnitus, vertigo
Path of the facial nerve
Exits brainstem at the cerebellopontine angle
Passes through temporal bone and parotid gland
Divides into 5 branches
- temporal
- zygomatic
- buccal
- mandibular
- cervical
What is the function of the facial nerve
Motor - muscles of facial expression, strapedius of the inner ear
Sensory - carries taste from anterior 2/3 of tongue
Parasympathetic - supply submandibular and sublingual salivary glands and lacrimal gland
Differentiating between upper and lower motor neuron facial nerve palsy
Each side of forehead has UMN innervation from both sides of the face
Each side of forehead has LMN from only one side of the brain
UMN - forehead will be spared (as it has dual supply)
Management of bells palsy
Prednisone (within 72 hours)
Lubricating eye drops
Not resolved within 3 weeks - ENT referral urgently
What is ramsay hunt syndrome
Facial nerve palsy caused by VZV
- look for rash over ear, pinna, inner ear
- tender painful rash
Treatment - prednisolone and acyclovir, also eye drops
Median nerve damage signs
Carpal tunnel
Sensory loss over first 3 and a half fingers and palm
Ulnar nerve damage signs
Elbow trauma Weakness / wasting of medial wrist flexor Interossei - cannot cross the fingers Claw hand Hypothenar wasting Sensory loss over ulnar fingers
Radial nerve damage findings
Compression at humerus
Wrist drop
Sensory loss variable
Sign of T1 root damage
Weakness in finger abduction
How long off driving if TIA or stroke if no neurological deficit
1 month
Epilepsy driving rules
Unprovoked/first seizure - 6 months off if no structural abnormalities or anything on EEG
If so, then 12 months
Drivers licence if 5 years no seizure in diagnosed epilepsy
What is cushings triad?
Widening pulse pressure
Bradycardia
Irregular breathing
Who is at risk of chronic subdural haematomas? Presentation
Alcoholics
Elderly
Several week fo months progressive history of either confusion, reduced consciousness or neurological deficit
Can be incidental finding
Management of TIA
300 mg aspirin for 2 weeks
75 mg clopidogrel long term
Secondary prevention- anti-hypertensive, diabetic modification, lipid modification
AF - anti coagulation
CAD - carotid endartectomy
T1 vs T2 MRI differences
T1 - fat is bright
T2 - fat and water is bright
Ptosis, down and out eye and dilated fixed pupil. What cranial nerve damage?
Oculomotor (CN III)
Defective downward gaze (vertices diplopia). Cranial nerve palsy? And its function
IV torchlear - eye movement
No corneal reflex Loss of facial sensation Sharp pain along face Paralysis of mastication muscles Deviation of jaw
What nerve palsy? Function?
V trigeminal
Facial sensation
Mastication
Defective eye abduction and horizontal diplopia, eye pulled inward which cranial nerve palsy? Functuon?
Abducens (VI)
Eye movement (lateral rectus)
IX nerve name and function
Glossopharyngeal
Taste (posterior 1/3 Rd of tongue)
Salivation
Swallowing
Weakness turning head in one direction, cranial neve palsy?
XI (accessory) on contralateral side
XII nerve name, function and what palsy may look like
Hypoglossal
Tongue deviated towards side of lesion
Uvula deviation, loss of gag reflex, difficulty swallowing which nerve palsy?
Vagus (X)
Uvula deviates away from site of lesion
Which cranial nerve cause uvula deviation?
Vagus (X) - deviates away from lesion
What cranial nerve palsy causes tongue deviation?
Hypoglossal (XII)
Deviates towarsds the lesion
Classical history of vestibular schwannoma
Combination of virtigo, hearing loss, tinnitus and absent corneal reflex (cranial nerve V)
Cranial nerve VIII - vertigo, unilateral sensineural hearing loss
What does C8 radiculopathy look like?
C8 dermatome lack of sensation - medial aspect of hand (little finger)
Weakness of flexion of distal interpahalgeal and metarcarpophalangeal joints)
Which is the only cervical nerve root that comes out below the vertebra?
C8
Features of Wernickes encephalopathy
Usually in alcoholics
Lack of B1
Confusion
Opthalmopegia/nystagmus
Ataxia
Classical symptoms of normal pressure hydrocephalus
Urinary incontinence
Dementia
Gait abnormality similar to parkinsons
Charcot Marie tooth disease features
Symptoms usually occur before aged 10 but onset of symptoms can be delayed until in 40s
Affects peripheral motor and sensory neurons
High foot arches (pes cavus) Distal muscle wasting Weakness in lowe legs - weak ankle dorsiflexion Reduced tendin reflexes Reduced muscle tone Perioheral sensory loss
Duchenne muscular dystrophy presentation
Progressive degeneration and weakness in specific muscle groups
Most patients lose ability to walk by aged 12
Most need resp support by 25
SENSATION INTACT
What is spared in MND?
Eye movements
What is progressive muscular atrophy?
Type of MND
LMN signs only
Affects distal muscles before proximal
Carries best prognosis
Fasiculations should make you think of what?
MND
Innervation of the eye muscles
All rectus apart from lateral and inferior oblique = oculomotor
Superior oblique = trochlear
Lateral lectures = VI abducens
Signs of cerebellar syndrome
DANISH
Dysdiadochokinesia Ataxia Nystagmus (horixontal) Intention tremor Staccato slurred speech Hypotonia
What is anterior inferior cerebellar syndrome?
Stroke of that artery
Ipsilateral loss of facial pain and temperature
Contralateral limb/torso pain and temperature loss
Ataxia nystagmus
What is webers syndrome?
Beaches of the posterior cerebral artery stroke
Ipsilateral CN III palsy
Contralateral weakness of upper and lower extremity
Further tests for someone less than 55 years old, presenting with stroke?”
Autoimmune and thrombophikia screening
Management of stroke associated with AF
2 weeks of aspirin
Switch to oral anticoagulation
If s stroke affects upper limbs more than lower limbs is it anterior or middle cerebral artery?
Middle
Anterior cerebral artery stroke presentation
Contralateral hemiparesjs and sensory loss affecting the lower limbs more than upper
No facial weakness or speech impairment
What measurement should be used to assess someone’s ability to return to daily activities after a stroke?
Barthel index
